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Diagnosis And Management > Pharmacology Week 7-9 > Flashcards

Pharmacology Week 7-9 Flashcards

1
Q

2 main divisions of autonomic nervous system

A
  • sympathetic

- parasympathetic

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2
Q

link between the CNS and peripheral organs

A

autonomic nervous system

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3
Q

What does the autonomic nervous system help regulate?

A
  • contraction and relaxation of vascular and visceral smooth muscle
  • all exocrine and certain endocrine secretions
  • the heartbeat

-energy metabolism(
liver and skeletal muscle)

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4
Q

what autonomic nervous system is closer to the end organ?

A

Parasympathetic “rest and digest”

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5
Q
  • active in resting phase
  • conserves energy
  • Acetylcholine ONLY
A

parasympathetic

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6
Q
  • fight or flight
  • energy expenditure
  • both acetylcholine and noradrenaline
A

sympathetic

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7
Q

What does parasympathetic nervous system do?

A
  • constricts pupils
  • stimulate saliva
  • slo heartbeat
  • constrict airways
  • stimulate activity of stomach
  • inhibit release of glucose, stimulates gallbladder
  • stimulate activity of intestine
  • contracts bladder
  • promote erection of genitals
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8
Q

What does sympathetic nervous system do?

A
  • dilate pupils
  • stimulate saliva
  • increase heartbeat
  • relax airways
  • inhibit activity of stomach
  • stimulate release of glucose, inhibits gallbladder
  • inhibit activity of intestine
  • secrete epinephrine and norepinephrine
  • relax bladder
  • promote ejaculation and vaginal contraction
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9
Q

All preganglionic nerve fibers are myelinated and release ______ from the nerve terminals

A

ACh

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10
Q

ACh produces excitatory postsynaptic potential in postganglionic neurons by activating ___________

A

nicotinic receptors

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11
Q

sympathetic postganglionic releases mainly__________

A

noradrenaline

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12
Q

parasympathetic postganglionic releases mainly__________

A

acetylcholine

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13
Q

what receptors are used for parasympathetic nervous system?

A

cholinergic receptors

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14
Q

What are the cholinergic receptors?

A

Muscarinic receptors

nicotinic

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15
Q

M1:
M2:
M3:

A
  • CNS and gastric parietal cells
  • heart
  • smooth muscle and glands
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16
Q

motor end plate, autonomic ganglia and adrenal medulla (targets)

A

nicotinic receptors

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17
Q

indications for local anesthetics:

A
  • infiltration, nerve block, epidural and intrathecal anesthesia
  • topical anaesthesia
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18
Q

lidocaine, benzocaine, prilocaine, cocaine examples of…..

A

local anesthetics

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19
Q

block impulse propagation and abolish sensations in a limited area

A

local anesthetics

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20
Q

What is the mechanism of action for local anesthetics?

A
  • blocking sodium channels in nerve membrane
  • drugs raise electrical excitation threshold (thus no action potential)
  • eventually slow and blocks the propagation
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21
Q

What are the sympathetic nervous system receptors called?

A

adenoceptors

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22
Q

different types of adenoreceptors?

A
  • alpha 1 (postsynaptic)
  • alpha 2 (presynaptic)
  • beta 1
  • beta 2
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23
Q

What is the different b/w beta 1 and 2 receptors?

A
  • beta 1: heart

- beta 2: bronchial (lungs)

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24
Q

describe the cholinergic junction (acetylcholine synthesis, release and signal breakdown)

A

1) acetylcholine is formed
2) packaged up in vesicles to lean the axon
3) released and crosses the synapse
4) binds to receptor activating a signalling cascade
5) cleared from synapse by acetylcholinesterase

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25
Q

acetylcholine is formed by an enzyme:

___________ + __________

A

Acetyl CoA + Choline

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26
Q 
activates muscarinic receptors, producing excitatory effects such as 
-
-
-
-
-
-
-
A

muscarinic agonists

  • miosis
  • sweating/ salivation
  • decrease in heart rate
  • bronchial constriction
  • increased GI motility/ relaxation of sphincters
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27
Q

if you block agonist receptors what would the effects be?

A

called an antagonist and the effects would be the inverse

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28
Q

neostigmine (myasthenia gravis) and donepezil (alzheimers)

A

anticholinesterases

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29
Q

breaks down acetylcholine

A

anticholinesterases

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30
Q

anticholinergics/ antimuscarinics

A

cholinergic receptors antagonists

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31
Q
  • not clinically useful for ANS (ganglion blockers)

- muscle relaxants act on the neuromuscular junction

A

nACh receptors antagonists

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32
Q

-parasympatholytic, antimuscarinic or anticholinergic drugs because they compete and block the action of Each at the muscarinic receptors

A

mACh receptor antagonists

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33
Q

adenoceptor agonists

A

sympathomimetics

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34
Q

main effects of receptor activation…
-alpha 1 receptors:

  • alpha 2 receptors
  • beta 1 receptors:
  • beta 2 receptors:
A
  • vasoconstriction
  • inhibition of transmitter release
  • increased cardiac rate and force (beta 1)
  • bronchodilation (beta 2)
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35
Q

asthma relievers (salbutamol) example of what type of sympathomimetics?

A

beta 2-adenoceptor agonist

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36
Q

adrenaline (EpiPen) example of what type of sympathomimetics?

A

alpha/ beta adenoceptor agonist

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37
Q

decongestants are example of what type of sympathomimetics?

A

alpha 1- adenoceptor agonist

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38
Q

drugs affecting the somatic nervous system?

A

botulinum toxins

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39
Q

drugs inhibiting acetylcholine release

A

presynaptic agents

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40
Q

inhibits the reuptake of noradrenaline (block NET)

A

stimulants (cocaine, amphetamines-used in ADHD)

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41
Q

increases noradrenaline release

A

stimulants

amphetamines-used in ADHD

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42
Q

blockers usually have the suffix ____

A

-lol

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43
Q

adrenoceptor antagonist examples

A
  • non selective beta blockers ( blocks beta 1 and 2)
  • selective beta 1 blocker (cardioselective)
  • non-selective beta-blockers (blocks alpha or beta)
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44
Q

how many deaths were due to cardiovascular disease (in 2017)

A

1 in 4

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45
Q

treatment of systemic hypertension, cardiac failure, shock, peripheral vascular disease, Raynaud’s disease and pulmonary hypertension

A

vasoactive drugs

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46
Q 
drugs that act on the heart are used for
-
-
-
-
A

-arrhythmias
-cardiac failure
-hypertension
-coronary insufficiency
(myocardial infarction and angina)

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47
Q

non-pharmacological management for hypertension:

  • lifestyle:
  • absolute risk:
A
  • lifestyle (exercise, smoking, cessation, diet, weight loss)
  • probability of cardiovascular event w/in 5 years), high cholesterol, diabetes, being obese/inactive
48
Q

management of hypertension (drug classes)

A
  • ACE inhibitor or angiotensin II receptor antagonist
  • calcium channel blocker
  • low-dose thiazide diuretic
49
Q

examples) captopril, Enalapril, ramipril

A

ACE inhibitors

50
Q

How do ACE inhibitors work?

A
  • low Na concentration juxtaglomerular cells secrete renin
  • goes into blood and angiotensin I is formed
  • angiotensin-converting enzyme in pulmonary blood (ACE) forms angiotensin II (which is what is blocked in ACE inhibitors)
  • causes vasoconstriction or aldosterone
51
Q

what happens if there is not enough angiotensin II?

A
  • decreased vasoconstriction; more vasodilation

- less resistant ; decreased blood pressure

52
Q

What does aldosterone stimulate?

A

stimulates sodium uptake on the cell

53
Q

What is the mechanism of action for ACE inhibitors?

A

blocks conversion of angiotensin I to angiotensin II

also inhibits breakdown of bradykinin

54
Q

what’s ACE stand for?

A

angiotensin converting enzyme

55
Q

what are the adverse effects of ACE inhibitors?

A

-non productive cough (due to increase in bradykinin)

56
Q

what are the main contraindications for ACE inhibitors??

A

pregnancy and renal failure

57
Q

What are the main drug interactions with ACE inhibitors?

A
  • loop diuretics
  • NSAIDs
  • sartans

all affect kidneys

58
Q

examples: candesartan, irbesartan, telmisartan

A

sartans: angiotensin receptor blocker

doesn’t block enzyme- blocks receptor

59
Q

What part of the pathway is broken down in tartan use for angiotensin?

A
  • low Na concentration juxtaglomerular cells secrete renin
  • goes into blood and angiotensin I is formed
  • angiotensin-converting enzyme in pulmonary blood (ACE) forms angiotensin II
  • (this part is blocked in sartans) causes vasoconstriction or aldosterone
60
Q

What is the mechanism of action for angiotensin receptor blockers (ARB)

A

competitive antagonist to type 1 angiotensin receptors

61
Q

what is a common adverse effect for ARB’s?

A

myalgia

62
Q

examples: dihydropyridine (-dipine) and non-dihydropyridine (verapamil and diltiazem)

A

calcium channel blockers

63
Q

What is the mechanism of action for calcium channel blockers?

A

reduce calcium entry into cells of myocardium, vascular smooth muscle, and cardiac conducting system by preventing L-type calcium channels from opening

64
Q

What are the adverse effects of calcium channel blockers?

A
  • flushing

- peripheral edema –> are usually prescribed diuretics but in this case they won’t work. (dihydropyridines)

65
Q

example: hydrochlorothiazide (HCT)

A

thiazide diuretics

66
Q

What is the mechanism of action for thiazide diuretics?

A

inhibits reabsorption of sodium and chloride in the proximal (diluting) segment of the distal convoluted time
-low doses –> vasodilator effect

67
Q

what are adverse effects to thiazide diuretics?

A

-weakness, muscle cramps

68
Q

What are contraindications for thiazide diuretics?

A
  • gout (can affects excretion of uric acid)

- diabetes

69
Q

suffix -lol

A

beta blockers

70
Q

what is the mechanism of action for beta blockers?

A
  • competitive antagonist of the beta- adrenergic receptor, decreasing HR, BP, and cardiac contractility
  • decrease renin production
71
Q

What are drugs used for heart failure?

A
  • ACE inhibitors, ARB
  • beta- blockers
  • loop diuretic (edema)
72
Q

Why are ACE inhibitors and ARB the first line therapy with beta blockers for heart failure?

A

the reduction in vascular tone decreased the work and oxygen demand of the failing heart

73
Q

increase the excretion of sodium and water useful for hypertension, HF, renal failure, nephrotic syndrome and cirrhosis

A

diuretics

74
Q

example: furosemide

A

loop diuretic

75
Q

What is the mechanism of action for loop diuretics?

A
  • potent diuretic (water tablets)
  • inhibit reabsorption of sodium and chloride in the ascending limb of the loop of Henle (inhibits Na/K)
  • fast and intense diuresis
76
Q

What are interaction with other drugs and loop diuretics?

A
  • drugs that cause hypokalaemia

- NSAIDs

77
Q

What are common adverse reaction for drugs used for arrhythmias?

A

potential to worsen the arrhythmia

78
Q

“white clots” platelet rich

A

arterial

79
Q

“red clots”

RBC and fibrin

A

venous

80
Q

inactivates coagulation process and inhibits development of clots

A

anticoagulants

81
Q

Vitamin K antagonists (anticoagulants)

A

Warfarin (Coumadin, Marevan)

82
Q

Factor Xa inhibitor (anticoagulant)

A

Aprixaban (eliquis) and rivaroxaban (xarelto)

83
Q

Direct thrombin inhibitors (anticoagulants)

A

dabigatran (Pradaxa)

84
Q

inhibits synthesis of Vitamin k dependent clotting factors (II, VII, IX, X) and antithrombotic factos protein C and S

A

warfarin

85
Q

What is a common adverse effect of warfarin

A

bleeding

86
Q

reversibly inhibits both free and fibrin-bound thrombin, preventing conversion of fibrinogen to fibrin, preventing thrombus formation

A

dabigatran

87
Q

What are adverse effects of dabigatran?

A

bleeding and gastritis/ dyspepsia

88
Q

(directly affects the cascade) selectively inhibits factor Xa, blocking thrombin to fibrin and thrombus development

A

rivaroxaban and apixaban

89
Q

Where do heparins work?

A

directly inhibit antithrombin part of cascade

90
Q

Where does dabigatran work?

A

directly inhibits thrombin IIa

91
Q

used in the management of arterial thrombosis (clots initially made of platelets) but not VTE (fibrin clots)

A

antiplatelets

92
Q

examples of anti platelets

A

aspirin (low dose)

clopidogrel (plavix)

93
Q

inhibits platelet aggregation by irreversibly inhibiting COX, reducing the synthesis of thrombin A2

A

aspirin

94
Q

What are common adverse effects of aspirin

A

GI irritation

asymptotic blood loss and increased bleeding time

95
Q

irreversibly binds to the platelet P2Y12 receptor and inhibits the platelet aggregation for the life of the platelet

A

clopidogrel

96
Q

improving the balance between myocardial oxygen supply and demand

A

antiangiinal drugs

  • Beta blockers
  • calcium channel blockers
  • nitrates (short/long acting)
97
Q

What is usually the first line therapy for stable angina?

A

beta 1- blockers

98
Q

glyceryl trinitrate, isosorbide denigrate, isosorbide mononitrate

A
  • shot acting nitrate

- long acting nitrates

99
Q

mediates vasodilation

-by reducing myocardium oxygen required by reducing venous return and preload to the heart

A

nitrates

100
Q

adverse effects of erythropoietin agonists

A
  • myalgia
  • hypertension
  • bone pain
  • headaches
  • peripheral oedema
101
Q

recombinant glycoprotein which binds to erythropoietin receptors and stimulates erythropoiesis (doping)

A

erythropoietin agonists

102
Q

drugs used in anaemia

A

folic acid, B12, iron, erythropoietin agonists

103
Q

required for synthesis of purine and pyrimidine bases (DNA) and for amino acid metabolism and normal erythropoiesis

A

folic acid

104
Q

adverse effects of folic acid

A
  • rash
  • sleep disturbance
  • no common adverse effects
105
Q

essencial for nerve development, unclean acid synthesis and normal erythropoiesis (necessary for absorption)

A

B12

106
Q

required for the formation of hemoglobin and myoglobin

A

iron

107
Q

common adverse effects of iron

A

-abdominal pain
=nausea
-vomiting
-constipation **

108
Q

what does erythropoiesis require?

A
  • iron
  • vitamin B12
  • folic acid
  • erythropoietin agonists
109
Q

What were the top 3 drugs prescribed in 2018?

A

1) rosuvastatin
2) atorvastatin
3) esomeprazole

110
Q

human monoclonal antibody and increases the number of LDL receptors by inhibiting their degradation by PCSK9 (evolocumab, alirocumab)

A

PCSK9 inhibitor

111
Q

what does PCSK9 inhibitor effect?

A

significantly decreases LDL- concentration

112
Q

ezetimibe
-blocks cholesterol transport protein in intestinal wall, without affecting the absorption of fat-soluble vitamins, bile acids, triglycerides

A

Cholesterol absorption inhibitor

-usually prescribed with statins (adverse effects common)

113
Q

What are the lipid lowering drugs?

A
  • HMG-CoA reductase inhibitors (statins)
  • cholesterol absorption inhibitors
  • PCSK9 inhibitors
114
Q

atorvastatin, fluvastatin, pravastatin, rosuvastatin, simvastatin

A

HMG-CoA reductase inhibitors (statins)

115
Q

limiting enzyme in cholesterol synthesis

A

HMG-CoA reductase

116
Q

what are indications for statin use?

A
  • high risk of coronary heart disease

- hypercholesterolaemia

117
Q

abnormal amounts of lipid in the blood

-lipoproteins are synthesized by _____

A

cholesterol

-liver

Diagnosis And Management (8 decks)

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